Surface Iron Inhibits Quartz-Induced Cytotoxic and Inflammatory Responses in Alveolar Macrophages

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• 作者：Mara Ghiazza ; Agnes M. Scherbart ; Ivana Fenoglio ; Francesca Grendene ; Francesco Turci ; Gianmario Martra ; Catrin Albrecht ; Roel P. F. Schins ; Bice Fubini
• 刊名：Chemical Research in Toxicology
• 出版年：2011
• 出版时间：January 14, 2011
• 年：2011
• 卷：24
• 期：1
• 页码：99-110
• 全文大小：373K
• 年卷期：v.24,no.1(January 14, 2011)
• ISSN：1520-5010

文摘

The mechanism of enhancement/inhibition of quartz toxicity induced by iron is still unclear. Here the amount of iron on a fibrogenic quartz (Qz) was increased by wet impregnation (Fe(NO₃)₃ 0.67 and 6.7 wt %). X-ray diffraction (XRD), XRF diffuse reflectance, UV鈭抳is, and infrared (IR) spectroscopies revealed dispersed ferric ions, and hematite aggregates at the higher loading. Surface features relevant to pathogenicity and cell responses were compared not only to the original quartz but also to reference quartz DQ12. Surface charge (味-potential) was more negative on the original and low-loaded specimen than on the high-loaded one. DQ12 had a less negative 味-potential than Qz, ascribed to the absence of aluminium present in Qz (1.7 wt %). All quartz specimens were able to generate HO^{鈥?/sup> radicals, iron-loaded samples being more reactive than original quartz. Iron deposition inhibited the rupture of a C鈭扝 bond. All quartzes were phagocytized by alveolar macrophages (AM桅 cell line NR8383) to the same extent, irrespective of their surface state. Conversely, iron loading increased AM桅 viability (evaluated by cytotoxicity and induction of apoptosis). Qz was found to be much less cytotoxic than DQ12. The induction of oxidative stress and inflammatory responses (evaluated by HO-1 mRNA expression and TNF-伪 mRNA and protein expression) revealed a reduction in inflammogenicity upon iron loading and a more inflammogenic potency of DQ12 ascribed to undissociated SiOH interacting via H-bonding with cell membrane components. The results suggest that besides aluminium also iron at the quartz surface may have an inhibitory effect on adverse health responses.}